Judgments of synchrony between auditory and moving or still visual stimuli.

The flash-lag effect is a visual illusion wherein intermittently flashed, stationary stimuli seem to trail after a moving visual stimulus despite being flashed synchronously. We tested hypotheses that the flash-lag effect is due to spatial extrapolation, shortened perceptual lags, or accelerated acquisition of moving stimuli, all of which call for an earlier awareness of moving visual stimuli over stationary ones. Participants judged synchrony of a click either to a stationary flash of light or to a series of adjacent flashes that seemingly bounced off or bumped into the edge of the visual display. To be judged synchronous with a stationary flash, audio clicks had to be presented earlier--not later--than clicks that went with events, like a simulated bounce (Experiment 1) or crash (Experiments 2-4), of a moving visual target. Click synchrony to the initial appearance of a moving stimulus was no different than to a flash, but clicks had to be delayed by 30-40 ms to seem synchronous with the final (crash) positions (Experiment 2). The temporal difference was constant over a wide range of motion velocity (Experiment 3). Interrupting the apparent motion by omitting two illumination positions before the last one did not alter subjective synchrony, nor did their occlusion, so the shift in subjective synchrony seems not to be due to brightness contrast (Experiment 4). Click synchrony to the offset of a long duration stationary illumination was also delayed relative to its onset (Experiment 5). Visual stimuli in motion enter awareness no sooner than do stationary flashes, so motion extrapolation, latency difference, and motion acceleration cannot explain the flash-lag effect. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neuroleptic-induced attenuation of brain stimulation reward in rats.

Tested a total of 85 male hooded rats in 3 experiments. In 30-min free-operant tests, the dopamine receptor blockers pimozide (.125, .25, and .50 mg/kg) and (+)-butaclamol (.1, .2, and .4 mg/kg) attenuated leverpressing for lateral hypothalamic brain stimulation. When discrete self-stimulation trials were offered in a straight alleyway, pimozide increased start box latencies, slowed running speeds, and reduced leverpressing rates. However, performance early in both lever-pressing and runway sessions was normal; performance deteriorated as testing progressed, following patterns that paralleled those seen when Ss were tested with reductions in the amplitude of stimulating current. Spontaneous recovery was obtained in both situations; experimenter-imposed 10-min timeouts caused renewed leverpressing and running. In contrast, alpha-noradrenergic receptor blockade by phenoxybenzamine (5, 10, and 20 mg/kg) failed to produce extinction-like response patterns. Data support the view that central dopaminergic systems are important components of the neural mechanisms mediating reward. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The substrate for brain-stimulation reward in the lateral preoptic area: III. Connections to the lateral hypothalamic area.

Double-pulse tests were used to estimate the refractory periods and anatomical linkage of the reward-relevant fibers that course between the lateral preoptic and lateral hypothalamic areas. In the 1st study, pairs of conditioning and test pulses were delivered to each site, and the interval between pulses varied; recovery from refractoriness was similar at both sites, with the curves generally rising from 0.6 to 2.0 ms. In the 2nd study, the pairs of pulses were delivered to both sites. Six of 7 rats showed evidence of axonal collision, with estimates of conduction velocity that ranged from 0.48 to 8.95 m/s across rats. These results suggest that a wide spectrum of fiber types characterizes the reward-relevant axons that course uninterruptedly between these 2 regions. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Integration of free pulses in electrical self-stimulation of the rat brain.

Frequency thresholds for electrical self-stimulation of the medial forebrain bundle were estimated in rats while low frequencies of pulses were applied continuously. When continuous pulses were delivered to the same electrode that received the 0.5-sec trains of response-initiated stimulation, thresholds decreased by the free-pulse frequency (Experiment 1), consistently across current (Experiment 2). Estimates of the reward added by concurrent, response-contingent stimulation of the opposite electrode of a bilateral pair predicted the drop in threshold caused by the noncontingent pulses applied to the opposite hemisphere (Experiment 3), again, robustly across test current (Experiment 4). Continuous pulses restricted to times between self-initiated trains lost their effect (Experiment 5). The perception of reward was invariant despite changes in the overall activity of the self-stimulation substrate. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Measuring threshold shifts for brain stimulation reward using the method of limits.

Thresholds determined from the frequency of pulses and the current for rewarding brain stimulation were obtained from rats with lateral hypothalamic electrodes. The threshold, defined as the frequency or current corresponding to one-half the maximum response rate, was interpolated from reward summation functions. Daily trials of both ascending and descending sequences of frequency and current yielded no significant difference between order of presentation. While there was more variability in the maximum response rates across the sessions, neither frequency- nor current-based threshold evaluations yielded significant rate effects. Findings suggest that the threshold procedure is generally not influenced by the sequence of delivery of stimulus values and, thus, may be regarded as a reliable measure of the reinforcing properties of brain-stimulation reward. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Temporal integration in self-stimulation: A paradox lost?

Seven self-stimulating rats with electrodes located along the medial forebrain bundle were used to study how excitation dissipates at the end of a train of rewarding electrical pulses. On a 5-s, fixed interval (FI) schedule, the rats pressed a lever to obtain 2 trains of pulses separated by gaps of up to 2 s; the first train was fixed at a just-subthreshold number of pulses, whereas the second train was used to scale the number of pulses needed to just support consistent responding. The number of pulses needed grew with increasing gaps between the 2 trains, rapidly at first and then decelerating to an asymptote, with time constants of a few tenths of a second. These results support C. R. Gallistel's (1974, 1978) model of leaky integration of rewarding brain stimulation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)